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Jay and colleagues show that TREM2 deficiency reduces the number of macrophages infiltrating the brain and is protective against disease pathogenesis in mouse models of Alzheimer’s disease.

Using Ezh2-deficient iNKT cells, Dobenecker et al. show that loss of H3K27me3 at the bivalently marked PLZF promoter is an essential link between TCR specificity and iNKT development in mice.

Jenkins et al. discover that failure of perforin and granzyme cytotoxicity by human and mouse CTLs/NK cells prolongs the immunological synapse, leading to repetitive calcium signaling and hypersecretion of inflammatory mediators that subsequently activate macrophages. Disengagement from target cells is dependent on apoptotic caspase signaling. The findings may provide mechanistic understanding for immunopathology in familial hemophagocytic lymphohistiocytosis.

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Takahashi et al. demonstrate that restoring glial glutamate transporter EAAT2 function improves cognitive functions and synaptic integrity while reducing amyloid plaques in a sustained fashion after treatment cessation.

Treatment with a new antibody against IL-17RB blocks pancreatic cancer metastasis and promotes survival in mice.

Ortiz et al. report the accumulation of immature myeloid cells in skin tissue of patients with inflammatory conditions, which predisposes to the development of cancer.

Expression of NLR family apoptosis inhibitory proteins (NAIPs) protect against the development of tumors in two models of colorectal cancer. Protection appeared to be independent of NLRC4 inflammasome activation

Liu, Nussenzweig, and colleagues track the differentiation of human progenitor cells into dendritic cells (DCs). They show that a granulocyte/monocyte/DC progenitor gives rise to a monocyte-DC progenitor that in turn gives rise to both monocytes and a common DC progenitor. The common DC progenitor produces the three major subsets of human DCs.

The Liu and Nussenzweig groups identify the immediate precursor of CD1c+ and CD141+ dendritic cells in the circulation of healthy donors. These precursor cells (hpre-cDC) were detectable in cord blood, bone marrow, blood, and peripheral lymphoid organs.

Tu et al. generated a novel CD160-deficient mouse and showed impaired NK cell–mediated tumor elimination and IFN-γ production. CD160+ NK cells are functionally distinct in secretion of IFN-γ from their CD160 NK cell counterparts.

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